Resumen
Prostate cancer (PCa) is the most common cancer in men and the second highest contributor to cancer deaths. Targeting lipid catabolism enzymes in PCa may offer new avenues for therapeutic approaches. During the last decade, carnitine palmitoyl transferase I (CPT1A) has been identified as a potential therapeutic target for a growing list of cancers. In this study, we have tested the hypothesis that excess CPT1A plays a key role in supporting adaptation to stress and antioxidant defense production in PCa cells. Specifically, we have studied molecular differences between CPT1A gain and loss of function models, revealing genetic and metabolic vulnerabilities that could be targeted to avoid progression to neuroendocrine differentiation, a lethal form of the disease. Examining public datasets, we have also found that excess CPT1A expression leads to worse progression-free survival in PCa patients.